宫颈癌的治疗进展

宫颈癌是全世界妇女中第二常见的恶性肿瘤,在非洲、亚洲以及南美洲,是妇女最常见的恶性肿瘤。其发病率和死亡率仅次于乳腺癌。宫颈癌的传统治疗是根治性手术（包括广泛全子宫切除＋盆腔淋巴结清扫术）和放疗,化疗主要用于晚期或复发转移的患者。近些年,随着科学技术的发展,其手术方式及放化疗方式都有了新的进展,同时,还出现了靶向治疗、基因治疗及疫苗预防等综合防治体系。     

宫颈癌患者心理干预研究进展

宫颈癌是女性常见的恶性肿瘤之一,多发生在50岁左右的女性。统计表明,我国每年新增宫颈癌患者10万人左右[1]。近几年国内外报道,宫颈癌发病率及病死率均有明显下降,但有年轻化的趋势,35岁以下的妇女宫颈癌发病率明显上升[2]。目前宫颈癌的治疗仍以手术为主,     

宫颈癌的中西医治疗现状

宫颈癌是女性常见的恶性肿瘤之一,现代医学主要通过手术、放疗、化疗等方式,其疗效值得肯定,与之对应的是毒副反应及并发症。中医将宫颈癌归属于"癥瘕"、"崩漏"、"带下病"等范畴,且对于其发病机制有独特的认识,中医药的方法治疗宫颈癌,不仅仅体现在增强免疫力、减轻毒副反应等方面,还体现在抗肿瘤、与放化疗同用增强疗效等方面。     

宫颈癌研究新进展

宫颈癌是威胁女性健康的最常见的主要恶性肿瘤之一,据统计全世界每年新发现有数万女性患有宫颈癌这种癌症,越来越多的妇女死于宫颈癌。宫颈癌也是一种预防的肿瘤,其致病因素多种多样,包括初次性生活的年龄、吸烟、HPV、HSV、HCMV、EBV等因素。目前的检测方法有巴氏涂片法、薄层液基细胞学涂片法、宫颈组织活检及宫颈管刮术、HPV-DNA检测、计算机辅助细胞学检测系统等方法可以诊断宫颈癌。早期诊断、早期检查对宫颈癌的预防和治疗具有积极作用,同时降低宫颈癌的死亡率。     

不容小觑的子宫内膜癌

子宫内膜癌,又叫子宫体癌,是妇科常见的恶性肿瘤之一,目前在国内发病率仅次于子宫颈癌。但是,由于生活方式的转变,其发病率在不断升高,并且随着宫颈癌筛查及预防的普及,在发达国家子宫内膜癌的发病人数已经超过宫颈癌,成为女性生殖道最为常见的恶性肿瘤。     

人乳头瘤病毒16型L1和L2晚期蛋白在原核细胞中的表达

目的　HPV的某些型别尤其是HPV16 ,18型感染与宫颈癌的发生有密切的关系。宫颈癌在全球妇女癌症死亡原因中居第二位。在发展中国家 ,宫颈癌在妇女癌症死因中列第一位。尽管早期宫颈癌患者放疗及手术治疗效果较好 ,但对中晚期宫颈癌患者治疗效果却很差。因而 ,采取有效的措施预防HPV感染对于宫颈癌防治工作无疑是非常必要的。在对乳头瘤病毒结构和功能的研究中发现 ,以L1和L2为保护性抗原构建的疫苗株很可能在预防HPV感染及其引起的恶性肿瘤方面发挥重要作用。目前国际上常通过原核和真核表达系统获得L1和L2蛋白。本实验拟通过原核表…     

子宫内膜癌手术治疗的研究进展

子宫内膜癌是妇科常见恶性肿瘤之一,手术是其主要的治疗方式。尽管开腹手术是治疗子宫内膜癌的传统方式,但随着医学科技的不断发展以及人们对术后生活质量要求的提高,妇科肿瘤的外科治疗方式也随之发生了革命性的变化。从传统开腹手术、腹腔镜手术、单孔腔镜技术,到2005年美国FDA批准应用于妇科手术的达芬奇机器人手术系统,子宫内膜癌的手术治疗方式也有了更多的选择。与传统开腹手术相比,微创手术凭借其创伤小、恢复快等优点,在子宫内膜癌的应用越来越广泛,但临床应用时间较短,仍需大样本多中心的长期随访研究来证实其安全性和有效性。本文主要围绕以上几种手术方式治疗子宫内膜癌的最新观点及研究进展进行综述。     

天然药物主要成分的抗宫颈癌作用机制

宫颈癌是威胁全球妇女健康及生命的主要恶性肿瘤之一.随着癌症理论的发展和临床耐药性的出现,开发探索高效低毒的抗宫颈癌药物逐渐成为宫颈癌治疗的研究关注点.本文就近年来一些表现出抗宫颈癌作用的天然药物成分多糖、皂苷类、黄酮类、生物碱类对宫颈癌抗肿瘤作用的研究进展及其潜在的药理机制作一综述,以期为开发高效低毒的抗宫颈癌药物提供...     

阴道微生态与免疫微环境的变化对宫颈癌的影响

宫颈癌是全世界妇女中第四大最常见的恶性肿瘤,持续感染高危型人类乳头瘤病毒(HR-HPV)是宫颈癌发生的主要原因。病毒会加重患者阴道微生态的紊乱程度,同时改变宫颈局部的免疫微环境,使病毒逃避机体的免疫监视,促进其在感染细胞内的增殖与扩散,导致宫颈癌的发生和发展。本综述将对近年来在HR-HPV的持续作用下阴道微生态与免疫微环境促进宫颈癌进展的研究进行分析,总结病毒免疫逃逸的机制,为防治宫颈癌的免疫治疗提供新思路。     

HPV感染与宫颈癌预防的研究进展

宫颈癌在全球范围内依然是严重威胁妇女健康的常见恶性肿瘤之一。流行病学调查显示,高危型HPV持续感染是导致宫颈癌发病的主要原因,并且HPV感染具有显著的特点,因此,预防HPV感染是防治宫颈癌的主要途径。已明确性行为是促进HPV感染最重要的辅助因子,个体免疫力低下及年龄因素亦是促进HPV感染的重要因素。研究显示,在全球逐渐开展的预防措施包括对常见的高风险HPV类型进行预防性疫苗接种及包括HPV检测在内的宫颈癌筛查项目的实施已经在降低宫颈癌的发病率方面起到了很重要的作用。近些年来,人们越来越重视HPV检测在宫颈癌筛查程序中的应用。由于HPV的感染率具有显著的地域性差异,我们需要针对各地区的特点以完善相应的宫颈癌筛查程序,从而为宫颈癌防治工作的开展提供重要依据。     

Curcumin as an anti-inflammatory agent: Implications to radiotherapy and chemotherapy

Cancer is the second cause of death worldwide. Chemotherapy and radiotherapy are the most common modalities for the treatment of cancer. Experimental studies have shown that inflammation plays a central role in tumor resistance and the incidence of several side effects following both chemotherapy and radiotherapy. Inflammation resulting from radiotherapy and chemotherapy is responsible for adverse events such as dermatitis, mucositis, pneumonitis, fibrosis, and bone marrow toxicity. Chronic inflammation may also lead to the development of second cancer during years after treatment. A number of anti-inflammatory drugs such as nonsteroidal anti-inflammatory agents have been proposed to alleviate chronic inflammatory reactions after radiotherapy or chemotherapy. Curcumin is a well-documented herbal anti-inflammatory agents. Studies have proposed that curcumin can help management of inflammation during and after radiotherapy and chemotherapy. Curcumin targets various inflammatory mediators such as cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor κB (NF-κB), thereby attenuating the release of proinflammatory and profibrotic cytokines, and suppressing chronic production of free radicals, which culminates in the amelioration of tissue toxicity. Through modulation of NF-κB and its downstream signaling cascade, curcumin can also reduce angiogenesis, tumor growth, and metastasis. Low toxicity of curcumin is linked to its cytoprotective effects in normal tissues. This protective action along with the capacity of this phytochemical to sensitize tumor cells to radiotherapy and chemotherapy makes it a potential candidate for use as an adjuvant in cancer therapy. There is also evidence from clinical trials suggesting the potential utility of curcumin for acute inflammatory reactions during radiotherapy such as dermatitis and mucositis.     

Melatonin and cancer: From the promotion of genomic stability to use in cancer treatment

Cancer remains among the most challenging human diseases. Several lines of evidence suggest that carcinogenesis is a complex process that is initiated by DNA damage. Exposure to clastogenic agents such as heavy metals, ionizing radiation (IR), and chemotherapy drugs may cause chronic mutations in the genomic material, leading to a phenomenon named genomic instability. Evidence suggests that genomic instability is responsible for cancer incidence after exposure to carcinogenic agents, and increases the risk of secondary cancers following treatment with radiotherapy or chemotherapy. Melatonin as the main product of the pineal gland is a promising hormone for preventing cancer and improving cancer treatment. Melatonin can directly neutralize toxic free radicals more efficiently compared with other classical antioxidants. In addition, melatonin is able to regulate the reduction/oxidation (redox) system in stress conditions. Through regulation of mitochondrial nction and inhibition of pro-oxidant enzymes, melatonin suppresses chronic oxidative stress. Moreover, melatonin potently stimulates DNA damage responses that increase the tolerance of normal tissues to toxic effect of IR and may reduce the risk of genomic instability in patients who undergo radiotherapy. Through these mechanisms, melatonin attenuates several side effects of radiotherapy and chemotherapy. Interestingly, melatonin has shown some synergistic properties with IR and chemotherapy, which is distinct from classical antioxidants that are mainly used for the alleviation of adverse events of radiotherapy and chemotherapy. In this review, we describe the anticarcinogenic effects of melatonin and also its possible application in clinical oncology.     

Neoadjuvant versus adjuvant treatment: which one is better for resectable esophageal squamous cell carcinoma?

ABSTRACT: Esophageal cancer is the eighth most common cancer worldwide, and especially in some areas of China is the fourth most common cause of death and is of squamous cell carcinoma (SCC) histology in >90% of cases. Surgery alone was the mainstay of therapeutic intervention in the past, but high rates of local and systemic failure have prompted investigation into multidisciplinary management. In this review, we discuss the key issues raised by the recent availability of esophageal SCC treatment with the addition of chemotherapy, radiotherapy, and chemoradiotherapy to the surgical management of resectable disease and discuss how clinical trials and meta-analysis inform current clinical practice. None of the randomized trials that compared neoadjuvant radiotherapy or chemotherapy with surgery alone in esophageal SCC has demonstrated an increase in overall survival in those patients treated with neoadjuvant radiotherapy or chemotherapy. Neoadjuvant chemoradiotherapy has been accepted recently for esophageal cancer because such a regimen offers great opportunity for margin negative resection, improved loco-regional control and increased survival. The majority of the available evidence currently reveals that only selected locally advanced esophageal SCC are more likely to benefit from the adjuvant therapy. The focus of future trials should be on identification of the optimum regimen and should aim to minimize treatment toxicities and effect on quality of life, as well as attempt to identify and select those patients most likely to benefit from specific treatment options.     

PF方案同步放化疗治疗中晚期宫颈癌的疗效及毒性反应研究

目的：探究PF 方案同步放化疗治疗中晚期宫颈癌患者的疗效和毒性反应。方法：回顾性分析我院在2014 年6 月～2015 年6 月期间收治的ⅡB～Ⅲ期宫颈癌患者,共152 例,根据治疗方法将其分为单纯放疗组和同步放化疗组,比较两组患者治疗的疗效 和毒性反应。结果：单纯放疗组和同步放化疗组近期疗效总有效率无显著差异,差异不具有统计学意义(P>0.05),但分别对ⅡB 和 Ⅲ期患者进行分析,Ⅲ期患者同步放疗组总有效率显著高于单纯放疗组,差异具有统计学意义(P<0.05);同步放化疗组患者治疗 后骨髓抑制白细胞下降和消化道反应发生率显著高于单纯放疗组,差异具有统计学意义(P<0.05),两组患者皮肤反应的发生情况 比较无显著差异(P>0.05)。结论：PF方案同步放化疗治疗Ⅲ期宫颈癌的临床疗效显著优于单纯放疗治疗,可有效提高近期总有效 率,毒性反应虽较单纯放疗组有所增加,但经临床支持治疗患者均可耐受。     

人源性食管癌异种移植模型的建立及应用进展*

食管癌是全球第十大常见癌症,其发病率和病死率较高,主要包括食管鳞状细胞癌(ESCC)和食管腺癌(EAC),通常发展到晚期才被诊断发现。食管癌的标准治疗方法包括放化疗、内窥镜疗法和外科手术,但其预后效果不甚理想。良好的动物模型可用于研究食管癌的发生发展和生物学机制。患者来源的异种移植(PDX)模型最大程度上保留了原始肿瘤的细胞形态、组织结构特征和与患者相似的遗传特征。PDX模型为研究食管癌患者对放化疗的反应性,寻求新的治疗靶点,改善预后效果提供了新的平台,使个性化精准治疗研究迈入新阶段。就食管癌PDX模型的特点、构建时常用的实验动物、优化模型建立的方法以及PDX模型在食管癌研究中的应用进行综述,并讨论了食管癌PDX模型的局限性和未来发展前景,以期为食管癌的个性化精准治疗、改善患者预后提供新的研究方向。     

乳腺癌化疗现状及相关研究进展

乳腺癌是除非上皮来源肿瘤中女性最常见的恶性肿瘤,在美国平均每3名女性中就有一名患乳腺癌,是女性肿瘤致死中的第二大原因,给政府经济造成了很大的损失。目前,乳腺癌主要是以手术治疗为主,而化疗,放疗等也作为相当重要的辅助治疗应用于临床。这种手术加化疗的治疗方法一直可以取得很好的疗效,甚至于可以保住乳房。近年来,乳腺癌的化疗已逐步成为其治疗的首选方式,包括术后辅助化疗和术前的新辅助化疗。但由于化疗药物的滥用和肿瘤本身的异质性或是其他原因,越来越多的肿瘤耐药性报道给乳腺癌的化疗带来了很大的挑战。而这种肿瘤耐药性的分子机制尚不是很清楚。本文将从乳腺癌的概述,乳腺癌化疗的现状及乳腺癌化疗的前景来综述这一灾难性疾病。     

Biomonitoring of the cytogenetic effect of antitumor therapy by means of micronucleus assay in exfoliated epithelial cells

Data are presented concerning the possibility of using the micronuclei (MN) level as a biomarker for cytogenetic effects in exfoliated epithelial cells of cancer patients under therapy. The number of MN in buccal cells of cancer patients under chemotherapy are very contradictory. A significant dose-dependent increment of MN in tumor and normal epithelial cells due to radiotherapy was shown in most investigations. Evaluation of MN induced by radiotherapy in exfoliated tumor cells can potentially identify the radiosensitivity of tumors and the outcome of treatment after the first fractions of irradiation. This technique is almost completely noninvasive and easily done in accessible primary cancers (oral cavity and uterine cervix). The text was submitted by the author in English.     

In vitro radiotherapy and chemotherapy alter migration of brain cancer cells before cell death

Although radiotherapy and most cancer drugs target the proliferation of cancer cells, it is metastasis, the complex process by which cancer cells spread from the primary tumor to other tissues and organs of the body where they form new tumors, that leads to over 90% of all cancer deaths. Thus, there is an urgent need for anti-metastasis strategies alongside chemotherapy and radiotherapy. An important step in the metastatic cascade is migration. It is the first step in metastasis via local invasion. Here we address the question whether ionizing radiation and/or chemotherapy might inadvertently promote metastasis and/or invasiveness by enhancing cell migration. We used a standard laboratory irradiator, Faxitron CellRad, to irradiate both non-cancer (HCN2 neurons) and cancer cells (T98G glioblastoma) with 2 Gy, 10 Gy and 20 Gy of X-rays. Paclitaxel (5 μM) was used for chemotherapy. We then measured the attachment and migration of the cells using an electric cell substrate impedance sensing device. Both the irradiated HCN2 cells and T98G cells showed significantly (p < 0.01) enhanced migration compared to non-irradiated cells, within the first 20–40 h following irradiation with 20 Gy. Our results suggest that cell migration should be a therapeutic target in anti-metastasis/anti-invasion strategies for improved radiotherapy and chemotherapy outcomes.     

Molecularly targeting the PI3K-Akt-mTOR pathway can sensitize cancer cells to radiotherapy and chemotherapy

Radiotherapy and chemotherapeutic agents that damage DNA are the current major non-surgical means of treating cancer. However, many patients develop resistances to chemotherapy drugs in their later lives. The PI3K and Ras signaling pathways are deregulated in most cancers, so molecularly targeting PI3K-Akt or Ras-MAPK signaling sensitizes many cancer types to radiotherapy and chemotherapy, but the underlying molecular mechanisms have yet to be determined. During the multi-step processes of tumorigenesis, cancer cells gain the capability to disrupt the cell cycle checkpoint and increase the activity of CDK4/6 by disrupting the PI3K, Ras, p53, and Rb signaling circuits. Recent advances have demonstrated that PI3K-Akt-mTOR signaling controls FANCD2 and ribonucleotide reductase (RNR). FANCD2 plays an important role in the resistance of cells to DNA damage agents and the activation of DNA damage checkpoints, while RNR is critical for the completion of DNA replication and repair in response to DNA damage and replication stress. Regulation of FANCD2 and RNR suggests that cancer cells depend on PI3K-Akt-mTOR signaling for survival in response to DNA damage, indicating that the PI3K-AktmTOR pathway promotes resistance to chemotherapy and radiotherapy by enhancing DNA damage repair.